Abeta peptide-induced toxicity is mediated through oxidative stress and is associated with an activation of intracellular signaling such as the redox-sensitive transcription factor NF-kappaB and MAPK pathways. We demonstrate on neuroblastoma cell line N2a that EGb 761 could prevent the activation of NF-kappaB, ERK1/2, and JNK pathways induced by Abeta. Furthermore, our results show that EGb 761 can also activate SIRT1. This activation could explain the reduction of NF-kB activity by promoting the deacetylation of Lys310 of subunit p65. On the other hand, aggregation of Abeta to insoluble fibrils is a crucial step in Abeta-induced neurotoxicity. Using fluorescence spectroscopy with thioflavin T and electron microscopy, we demonstrate that EGb 761 and its flavonoid fraction (CP 205) could prevent the Abeta fibril (fAbeta) formation in vitro. Finally we show that Abeta is less toxic to N2a neuroblastoma cells when the peptide is previously incubated with the flavonoid fraction or EGb 761 during the fibril formation period. On the other hand, the ginkgolide compound BN 52021 was not able to prevent fAbeta formation. Interestingly it could also protect cells against Abeta toxicity. Our study demonstrates that the protection of neuronal cells by EGb 761 against Abeta could involve different mechanisms as the regulation of several key intracellular pathways and the inhibition of fAbeta formation and implicate more than its free radical scavenging property.
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http://dx.doi.org/10.1016/j.freeradbiomed.2006.08.015 | DOI Listing |
Brain Sci
December 2024
Epidemiology, IQVIA, 60549 Frankfurt am Main, Germany.
Background/objectives: Previous research indicates that extract (Gbe) may contribute to slowing down the progression of dementia. This retrospective cohort study analyzed the association between Gbe prescriptions and the progression of dementia severity in a real-world setting.
Methods: This study was conducted using data from patients with an initial diagnosis of mild or moderate dementia between January 2005 and December 2022 from the IQVIA™ Disease Analyzer database.
J Inflamm Res
January 2025
Key Laboratory of Ministry of Education for TCM Viscera-State Theory and Applications, Liaoning University of Traditional Chinese Medicine, Shenyang, 110847, People's Republic of China.
Purpose: Myocardial infarction (MI) is a prevalent cardiovascular disorder affecting individuals worldwide. There is a need to identify more effective therapeutic agents to minimize cardiomyocyte damage and enhance cardioprotection. extract is extensively used to treat neurological disorders and peripheral vascular diseases.
View Article and Find Full Text PDFAm J Ther
January 2025
Faculty of Medicine, "Transilvania" University, Brasov, Romania; and.
Background: Dementia leads to cognitive decline affecting memory, thinking, and behavior. Current pharmaceutical treatments are symptomatic, with limited efficacy and significant drawbacks. Ginkgo biloba extract (EGb761) is being explored as an adjuvant therapy for dementia because of its potential neuroprotective effects.
View Article and Find Full Text PDFPhytomedicine
January 2025
Department of Psychiatry and Psychotherapy, University Medical Center Mainz, Johannes Gutenberg-University Mainz, Mainz, Germany; Research Center for Immunotherapy (FZI), University Medical Center at the Johannes Gutenberg University Mainz, Mainz, Germany. Electronic address:
Background: Ginkgo biloba leaf extract EGb 761® has shown clinical efficacy in patients with mild cognitive impairment and dementia. However, the pharmacological action of EGb 761® in Alzheimer's disease (AD) remains unclear and molecular mechanisms targeted in the brain are not completely understood.
Hypothesis/purpose: We aimed to investigate 1) the potential sex-dependent effects of oral administration of EGb 761® in 5xFAD mice, an AD mouse model, and 2) the underlying microglial subtype responsible for the observed anti-inflammatory effects in the brain.
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